psychobio 3 Flashcards

set point range

a single value that the body works to maintain
ex: calcium level, temperature, water, etc.

weight is regulated tightly within a...

set point range

energy imbalance

when weight consistently increases or decreases


one of the top 5 health problems - a mass epidemic
many health risks with being over or under weight

body mass index

a measure of body fat
= body weight/ height^2
more than 1 in 3 adults are obese

mortality rates and BMI

thinner people live longer
very thin people do not have the lowest mortality rates,
average BMI has the lowest risk

estimations for BMI

BMI is dependent on weight and height so it makes simplistic
assumptions about distribution of muscle and bone mass

overestimated for more lean body mass - athletes

underestimated for less lean body mass - elderly

central deposition of fat (central obesity)

you have greater health risks if you have excess fat in your waist -
if your waist circumference is more than half your height, you have
dangerous visceral fat

dangers of visceral fat

visceral fat releases toxic substances and causes metabolic diseases
associated with central obesity - hypertension, high cholesterol, type
2 diabetes, coronary heart disease

function of digestive system

to break down food into smaller molecules that the cells can use

how does digestion work

begins in the mouth where saliva enzymes break down carbohydrates
hydrochloric acid and stomach enzymes digest proteins
small intestine enzymes digest proteins, fats and
carbohydrates and absorb the digested food into the bloodstream
large intestine absorbs water and minerals and lubricates
remaining materials to be excreted


controlled stability of the internal environment of cells and tissues
biological processes that keep body variables within a fixed
range or set point

feedback control loops

explained how certain systems work as homeostatic mechanisms

claude bernard

father of modern experimental physiology
-studied digestion and role of pancreas
-understanding of glucose regulation in the liver
discovered neural control of blood vessels

negative feedback processes

processes that reduce discrepancies from the set point
when something becomes off in the body, negative feedback
loops work to bring it back to normal
ex: when you eat, glucose levels rise so insulin is released
to regulate glucose levels

what contributes to hunger and feeding behaviors

a combination of learned and unlearned factors
ex: food selection, hunger, appetite, satiety


the stimulus that drives our need to eat
when our bodies need fuel, signals are sent from the empty
stomach and intestines that trigger our feelings of hunger

human vs animal strategies of eating

humans tend to eat more than they need
most animals will eat only what they need
alaskan chickadee eats 10% of its body weight per day and
shivers it off at night
bears will eat as much as they can and wont stop so they have
enough storage for hibernation and live off their excess fat

signals of hunger

processed by the brain, but can be overrided
1. delay hunger response actions - people who fast or starve
usually have lower hunger
2. eat more than we need by ignoring satiety receptors that
signal fullness


a type of signal to eat - can have an appetite for food with or
without hunger
ex: you could have eaten not long ago but sights, smells,
thoughts or discussion of food can stimulate appetite


stressful situations often stimulate appetite (stress-eaters)
food is comforting and those who are experiencing episodic or
chronic stress find comfort in eating
emotionally stressful situations may lead to periods of
binge-like eating in some individuals


the feeling of fullness that stops appetite and hunger signals
the brain regulates eating through messages from the mouth,
stomach, intestines, fat cells and elsewhere

why is it easy to sometimes overeat

satiety signals that originate in the stomach are delayed from the
start of eating so sometimes you eat more than you need to before
satiety signals are received and acted upon

gastric bypass surgery

the removal or sewing off of part of the stomach
decreased stomach size allows distention of the stomach and
produces satiety sooner

proof that stomach distention is not the only satiety signal

people who have had their stomach removed surgically (ex: cancer)
still report satiety, so signals have to be coming from elsewhere
rather than just the stomach

oral factors of hunger and satiety

the desire to taste and have mouth sensations like chewing cause hunger
people who have a tube in their stomach for feeding report not
feeling satisfied when being fed because they need to chew something
untasted meals are unsatisfying

how are hunger signals affected by the foods you eat

the length of time food stays in the stomach and intestine affects
the duration of satiety and initiation of hunger signals

foods high in protein and fiber vs foods high in fat and processed sugars

foods high in protein and fiber have a high satiety value because
they take longer to digest and stay in the stomach and intestine longer
processed/fatty foods have a low satiety value because they
are easily digested and absorbed readily, they fail to trigger
satiety signals
whole grain products cause people to feel no hunger because
their satiety signals remain on

stomach wall stretching

information conveyed by the vagus nerve to the brain, providing the
major basis for satiety

stomach nutrient content

conveyed by the splanchic nerves


the part of the small intestine adjoining the stomach
the first digestive site that absorbs a significant amount of nutrients
releases CCK and GLP-1

CCK and GLP-1

released by the duodenum to restrict flow through the duodenum
causing the stomach to slow gastric emptying and facilitates stomach
distension (the primary signal for ending a meal)
both signal the brain satiety mechanisms

what happens in a healthy person after they eat

glucose levels rise due to the intake in
carbohydrates, if not used, liver cells convert some of the excess
glucose into glycogen for later use and fat cells convert it to fat

insulin levels rise due to the signals of excess
glucose in the body and insulin is released from the pancreas and
enables the glucose to enter the cell - decreases blood glucose and appetite

what happens in between meals

insulin levels are low - hunger is highright before you eat,
insulin is highest and preparing to use the glucose you intake from food
glucose levels are low - glucagon is released and liver cells
convert glycogen back into glucose which returns to the blood and
slows the return of hunger

arcuate nucleus

part of the hypothalamus that has one set of neurons sensitive to
hunger signals, and another set sensitive to satiety signals

damage to the LH results in..

loss of appetite

difference between appetite and hunger

you can have an appetite without being hungry!
appetite is initiated by being hungry, but can also be
stimulated by seeing, hearing, smelling food whether you are hungry
or not
hunger is your body's way of telling you it is actually
hungry, not just an appetite from seeing something delicious


lowers hunger, highest levels right after you ate a big meal
low leptin levels trigger hunger, high leptin levels trigger satiety

Leptin Lowers hunger


levels increase before a meal to signal hunger and trigger stomach contractions
released by the stomach in a time of food deprivation
the only known hunger hormone

Ghrelin Grows hunger

signals that trigger hunger

taste pathways
decrease in leptin levels
increase in ghrelin

signals that trigger satiety

release of CCK (signal for ending a meal)
increase in leptin levels
rise in blood glucose and insulin

arcuate nucleus pathway for hunger

hunger signals in ARC inhibit the PVH which stimulates the LH to
allow for eating

arcuate nucleus pathway for satiety

satiety signals in ARC stimulate the PVH which inhibits the LH to
stop eating

lateral hypothalamus

facilitates feeding - when stimulated, eating is increased
when inhibited, feeding is stopped

paraventricular hypothalamus

works with (hunger or satiety) signals from the arcuate nucleus to
either stimulate the LH to increase feeding, or inhibit the LH to stop feeding

inhibition of the PVH leads to...

stimulation of the LH and an increase in feeding

stimulation of the PVH leads to...

inhibition of the LH and a stop in feeding

where do all of the signals for feeding occur

in the hypothalamus

inhibitory feeding transmitters

NPY, AgRP and GABA released from hunger signals in the ARC to inhibit
PVH and stimulate LH to stimulate eating
THINK OPPOSITE - inhibitory transmitters stimulate the LH
work on the PVH to excite the LH!!

excitatory feeding transmitters

melanocortin - released from satiety signals in the ARC to stimulate
PVH and inhibit LH to prevent eating
THINK OPPOSITE - excitatory transmitters inhibit the LH
work on the PVH to inhibit the LH!!

leptin hypothesis

high leptin inhibits hunger so some obese persons have a genetic
inability to produce leptin (leptin synthesis deficit) which leads to
more hunger
some obese persons have leptin resistance so they perceive
less leptin than is present and leads to more hunger

melanocortin hypothesis

melanocortin normally excites the PVH to inhibit the LH to stop
eating, some obese persons have a mutated melanocortin receptor gene
so they overeat and become obese because their PVH is not able to
receive the satiety signal

ventromedial hypothalamus (VMH) hypothesis

some persons have damaged VMH leading to excessive eating
increased gastric emptying leads to decreased satiety
increased insulin release and fat storage
both of these effects result in an increase of hunger and eating

emotions can...

enhance communication with other's and with oneself
color experience by focusing one's attention in certain
directions or motivate a person to behave in particular ways

the six basic emotions

anger, sadness, disgust, fear, happy surprise

tripartite mind-body interaction

cognitive awareness of objective events leads to emotional,
physiological and behavioral response

the brain uses ____ to convey the physiological response

autonomic nervous system

4 theories of emotion

common sense theory, james-lange theory, cannon-bard theory,
schacter-singer theory

common sense theory of emotion

emotion comes first, then a specific pattern of autonomic arousal and
skeletal action occurs
frightening situation -> FEAR -> action (running away,
increased heart rate, etc)
"i tremble because i feel afraid

james-lange theory of emotion

autonomic arousal and skeletal actions come first, then we experience
the emotion
frightening situation -> action (running away, increased
heart rate, etc) -> FEAR
main contribution - the experience of emotion may involve
"reading" the state of one's own body
"I feel afraid because i tremble

cannon-bard theory of emotion

emotion is produced in the brain alone, the emotion is mediated via
brain activity following processing of sensory information
emotional cognition, autonomic arousal and skeletal action
occur simultaneously
"the dog makes me tremble and feel afraid

schacter-singer theory of emotion

nonspecific feelings of physiological arousal occur and then
emotional labels are attributed to them
the CNS interprets the current social, physical and cognitive situation
the physiological response is a cue to the brain that something
important may be happening to us
"i label my trembling as fear because i appraise the
situation as dangerous

schacter-singer - the vitamin "suproxin" study

hypothesis: would participants be deceived into experiencing a mood
based on available "cognitive circumstance" in the absence
of an appropriate explanation for arousal?
gave a dose of adrenaline to college students and gave a
placebo to the other and told some of them that the medication was
going to make them aroused. They were placed in a room with a
confederate who was either happy or angry and the ones that were told
they were going to have a physiological response showed anger or
happiness like the confederate in the room with them, placebo showed
no response

what are key components of emotion mechanisms

interpretation of physical states (facial expressions, physiological changes)

what are the critical areas for producing emotion

the limbic system and forebrain
other brain scans have shown areas of the cerebral cortex and
frontal and temporal lobes also activated during an emotional experience

limbic system

the forebrain areas surrounding the thalamus - consists of a number
of interlinked structures that form a border around the brainstem
mediates emotion, motivation, aggression, learning and memory

what did james papez hypothesize

that emotional experience was primarily determined in the cingulate
gyrus and prefrontal cortical regions
but emotional expression is not just the function of one
specific brain center, it is the result of a circuit of limbic system structures

phineas gage

tampering rod went through his brain, took out the connections
between the frontal lobe and the limbic system
used to be a fun, loving guy - then became an aggressive, no
filter, mean guy after the rod took out the connections
showed that higher order structures inhibit lower order
structures - prefrontal cortex could not regulate limbic system so
his emotions were sporadic

how do the limbic system and frontal lobe work together

inhibitory connections from the prefrontal cortex to the limbic
system suppress its emotional suggestions

consequences of damage to the prefrontal cortex

impairs decision making and results in hyper-emotionality (ex:
phineas gage)
loss of prefrontal cortex control leads to impulsive decision
making without considering the consequences
inability to anticipate the unpleasantness of an outcome

ADHD - attention deficit hyperactivity disorder

5% of children or more, 2-3x more in boys
symptoms - distractibility, impulsiveness, hyperactivity
delay in prefrontal cortex cortical development
treated with serotonin reuptake inhibitors to enhance limbic
inhibition and ritalin to block reuptake of dopamine

which hemisphere is more responsive to emotional stimuli

the right hemisphere - listening to laughter or crying activates the
right temporal lobe amygdala more than the left
viewing pictures of emotional facial reactions (anger, fear,
sadness, happiness, disgust) activates the right temporal cortex more
than the left

damage to the right temporal cortex

causes deficits in identifying emotional expressions of others


a key structure in the mediation of fear
informs of potential dangers in the environment
many of our body's alarm circuits are grouped together and
linked to the amygdala

function of fear

to alert us of danger

function of anger

directs us to attack an intruder

function of disgust

tells us to avoid something that could cause illness

study with amygdalectomized monkeys

monkeys who had their amygdalas cut out showed higher social
affiliation, lower anxiety, high confidence and lower reluctance to
engage a strange monkey in social behavior
overall, they were less fearful

damage to the amygdala interferes with...

learning of fear responses
retention of previously learned fear responses
interpreting stimuli with emotional responses (ex: a
threatening stimuli)

behavioral medicine

extension of biopsychology toward health, emphasizes the effects of
emotions and other behaviors (diet, exercise, smoking) on health and illness
major focus - relationship between life distress and disease -
potential ways stress may affect disease


non-specific response of the body to any demand made upon it
the process by which we perceive and respond to events that are
perceived as harmful, threatening or challenging
10 leading occupational health problems in the US
each of us experience stress in our daily lives, without it our
lives wouldbe dull but when stress overtaxes our coping resources, it
can damage our health

working hypothesis of the stress-disease relationship

chronic and/or repeated acute stress adversely affects multiple
physiological symptoms and contributes to disease pathophysiology more
readily in susceptible persons
aka - more/repeated stress leads to greater disease

sources of stress

major life events, catastrophes, daily hassles, environmental, job-related


any event or situation that triggers coping adjustments


the adaptive process of achieving stability (homeostasis) through
physiological or behavioral change
can be carried out by alteration internal regulatory systems
is essential for maintaining internal viability and changing conditions

allostatic load

cumulative long-term effects of the body's physiological response to
stress. both repetitive acute and prolonged chronic stressors may contribute

the stress stimulus

common elements to situations that may elevate stress responses in everyone
- novelty- unpredictability- threat to the
ego- loss of control

the stress response - walter cannon

flight or fight response"
showed extensive research on the bodily response to stressors
(ex: temp extremes, oxygen deficit, negative emotions)
the mind and the body are not discrete and unrelated, they
greatly influence each other
stress is a gift to be used wisely, helps people overcome adversity
major emotions involve the excitation of the nervous system

flight or fight response

prepares the body for handling brief emergencies
induced by stress
brought about by the activation of the
hypothalamic-pituitary-adrenal cortex (HPAC) axis and the
sympathetic-adrenal medulla (SAM) axis

hans selye

defined stress as the non-specific response of the body to any demand
made upon it
studied influence of stress on ability to cope with and adapt
to the pressures of injury and disease
discovered that a variety of ailments became apparent with
similar symptoms, attributed to the body's efforts to respond to the
stresses of being ill

general adaptation syndrome

any threat to the body activated a generalized response to stress

eustress" - good stress

when stressors are viewed as challenges, then they can lead to growth
and enhanced functioning

3 stages of general adaptation syndrome

1. alarm stage
2. resistance stage
3. exhaustion stage

alarm stage of general adaptation syndrome

acute increase in sympathetic nervous system activity, readying the
body for brief emergency activity

resistance stage of general adaptation syndrome

sympathetic response declines, adrenal cortex releases cortisol and
other hormones that enable the body to maintain prolonged alertness,
fight infection and heal wounds
highest resistance to stress

exhaustion stage of general adaptation syndrome

occurs after prolonged stress when the nervous and immune systems no
longer have the energy to sustain heightened responses
inactivity, vulnerability and decreased energy to sustain
heightened responses

when is cortisol released

in the resistance stage of the general adaptation syndrome
enables the body to maintain prolonged alertness, fight
infections and heal wounds

activation of general adaptation syndrome

activated by long-term, inescapable factors
in the short term is helpful, in the long term is harmful to health

HPAC axis

hypothalamic-pituitary-adrenal cortex
becomes the dominant response to prolonged stressors
activation of hypothalamus induces the pituitary gland to
secrete adrenocorticotrophic hormone (ACTH)
ACTH stimulates the adrenal cortex to secrete cortisol


stimulates the adrenal cortex to secrete cortisol


stress hormone"
helps to mobilize energies to combat a difficult situation
levels of cortisol are used as an index of stress - more
cortisol means you're overcoming more stress

the transactional model

richard lazarus - the experience of stress depends as much on how an
event is appraised as it does on the stressor event itself
"our emotions and thoughts are inextricably linked"
when we are presented with a stressor, we appraise the
situation as not harmful, or harmful. if harmful, we cope with it and
deal with the aftereffects and wear and tear


study of the relationship of psychological and behavioral factors,
immunity and changes in health status

flight or fight response is driven by...

the central nervous system

ader and cohen study

were studying rats with conditioned taste aversion to a
nausea-inducing drug
gave rats sugar water then injected a nausea inducing drug
later found that the rats were getting very sick and dying
because the taste of the sugar water produced a conditoned response
that produced a weakened immune system
later discovered that the number of virus and infection
fighting immune cells was significantly reduced, this led to proof
that the brain and immune system were connected

2 responses to stress

1. sympathetic (inside autonomic) nervous system is activated - fight
or flight response
2. HPAC axis activated - hypothalamus is activated which
induces the pituitary gland to release ACTH, which then stimulates
the adrenal cortex to release cortisol

exam stress

students had lower antibodies during exam times than during vacations

lonely students

lonely students had poorer immune function than non-lonely students
during exams

perceived stress

exposed subjects to cold virus; those who had 1 month or more of
increased perceived stress were more likely to become infected

nuclear accident

residents within 3 miles of the nuclear accident had lower immune
system function 6 years later relative to those without elevated
perceived stress

effects of long term stress on the immune system

release of substances that injure cells and cause an elevation of
inflammatory cytokines in the body - this produces symptoms of illness
(ex: fever, sleepiness, lack of energy, etc)
sleep and inactivity are the body's way of conserving energy to
fight illness

negative emotions, inflammation and stress

inflammatory substances are linked with depression, fatigue and other
negative emotions
negative emotions contribute greater risk for prolonged
infection and delayed wound healing which further fuels sustained
inflammatory substance release

causes of amnesia

amnesia - the loss of memory
many kinds of brain damage, caused by disease or accident,
impair learning and memory and cause amnesia

anterograde amnesia

the inability to form new memories after the event that caused the amnesia

retrograde amnesia

loss of memory for information occurring prior to the event that
caused the amnesia

HM study

underwent an experimental brain surgery for seizures and after the
surgery he could not make any new memories (suffered from anterograde amnesia)
surgery was a bilateral temporal lobe resection, which included
amygdala and some surrounding cortex
could not make new memories or every day events and could not
learn new information, but had good short term memory
did not suffer from any intellectual or personality disorders,
despite his amnesia

outcome of HM study

because HM only suffered from anterograde amnesia and did not lose
any of his short term memory, past memory, personality or intellectual
ability, researchers hypothesized that the hippocampus was necessary
for forming new memories, but may not be where new memories are stored

job of the hippocampus

to serve memory consolidation for declarative memory, not LTM storage
memory consolidation is transferring short term memory into long
term memory

hippocampus damage

in the case of HM or a lesion - it impairs recent learning more than
older learning
people with hippocampus damage can learn new skills but have a
hard time learning new facts

delayed non-matching-to-sample task

a declarative memory task - an animal must learn that of the two
objects, the food is under the one it had not seen 10 minutes before
when the animal has hippocampus damage, they are still able to
learn the correct response when there is no delay, but damage impairs
their memory consolidation, causing forgetting after 10 minutes

declarative (explicit) memory

facts and info acquired through learning that can be consciously recalled
we are aware of this info and we can declare or verbalize it to
others - deals with "what

nondeclarative (implicit or procedural) memory

previous experiences aid the performance of a task without conscious
awareness of these previous experiences.
memory about perceptual or motor procedure, demonstrated by
performance rather than by conscious recollection - deals with the "how

2 types of declarative memory

episodic - recalling a specific episode in your life
semantic - basic facts acquired over a lifetime

3 forms of nondeclarative memory

skill learning

skill learning

type of nondeclaritive memory
learning to perform a series of procedures that requires motor coordination
ex: people were told to trace an image but can only see the
mirror reflection. normal people improved with practice, people
with deficits in nondeclarative memory could not show improvement
with practice

priming (repetition priming)

type of nondeclaritive memory
improvements in a behavioral response when stimuli are
repeatedly presented
or: exposure to a stimulus facilitates or speeds subsequent
responses to the same/similar stimulus


type of nondeclaritive memory
learning simple associations between two stimuli, or a stimulus
with a response
pavlovian or operant

classical (pavlovian) conditioning

the pairing of two stimuli changes the response to one of them
UCS automatically leads to UCR, but with repeated pairing of the
CS with the UCS, soon the CS will produce the CR
think pavlov's study with dogs and salivation

operant conditioning

responses are followed by reinforcement or punishment that either
strengthen or weaken the probability of the behavior occurring in the future
positive and negative reinforcers are events that increase the
probability of the response occurring again
punishments are events that decrease the probability that the
response will occur again
think watson and skinner

short term memory

memory of events that have just occurred
STM retains info for less than a minute if attention is paid to
the elements in sensory register
repetition keeps the info available longer

long term memory

memory of events from times further back
memory trace - a persistent change in the brain that reflects
the storage of info
neuronal activities continue even after the termination of the
stimulus - inducing structural changes
different neurons are linked via this activity and form neural
circuits that can fire in specific patterns with minimal stimulation

sensory memory

briefest memories are called iconic (visual) and echoic (auditory) memories
they are fleeting impressions that vanish within a second,
thought to be residual sensory perceptions

3 aspects of info processing for a functional memory system

encoding of raw info from sensory channels into STM

consolidation of volatile STM traces into more
durable LTM

retrieval of stored info for use in future behavior
problem with any of these leads to forgetting

working memory (central executive)

responsible for the transient holding and processing of new and
already stored information; integral for reasoning, comprehension and
learning and memory

lashley's search for the engram

engram - the physical representation of what has been learned
lashley trained rats on different mazes and then cut or removed
various parts of their brains to see if any cuts or lost parts would
cause them to forget how to do the maze. his research led him to
believe that
1. all parts of the cortex contribute equally to learning and
complex behaviors and
2. the cortex works as a whole, and more cortex is better
researchers later discarded these assumptions with more research

studies of memory retrieval

show that memory retrieval from LTM causes memories to become
temporarily unstable and susceptible to disruption or alteration
before reconsolidation
ex: people recalling facts for a jury
but using memories again makes them plastic again and
suscepitble to updating

hippocampus and context

hippocampus is involved in cognitive processing of space, time and
the relationships of external cues occurring at the time of an
event...contextual learning
ex: remembering the detail and context of an event

cognitive map

term is coined by tolman
studied learning using mazes and rats
concluded that learning did not result strictly from a stimulus
and a response - but rather through more subtle differences of
processing of info where prior experiences and connections could be
applied to new situations
hippocampus damage impairs spatial learning

test used to asses spatial ability in rodents

radial maze - navigate a maze with 8 or more arms, with a reinforcer
at the end of selected arms
studies showed that animals do not just learn a series of turns,
but instead develop a cognitive map to do the maze

radial arm maze

8 arms with food at a selected few - tested rodents with and without
hippocampus damage to see if they could remember which arms they
already went to to get food
must use extra-maze cues to determine which arms have been
entered during a particular trial (STM) and enter each baited arm
only once following training (tests working/LTM)

results of radial arm maze with rats

separate trained rats underwent lesioning in several different parts
of the brain including the hippocampus, but only rats with damage to
the hippocampus were impaired
place cells fire in radial maze study to show rats where they
are relative to the environment - this lets them see where they've
been and where they haven't

cognitive map

a mental representation of the spatial layout of an environment made
up of boundary, place and grid fields
boundary cells-fire when a person is located near the geographic
limit of the space they are in

place cells-fire when persons occupy a particular location
relative to the arrangement of objects within an environment
grid cells-fire when the person is in, or moving toward, a
particular location

prefrontal cortex and anterior cingulate cortex involvement in
learning and memory

liked to learning about rewards and punishments

parietal lobe secondary cortex involvement in learning and memory

associated with piecing sensory and motor information together

anterior and inferior region of the temporal cortex involvement in
learning and memory

associated with semantic memory (meaning of words) and object recognition

erik kandel

studied the gill and siphon withdrawal reflexes in aplysia, chose
aplysia because of the simplicity and relatively large size of the
neural circuitry
studied habituation, dishabituation and sensitization

results of kandel's study with aplysia

provided solid evidence for the mechanistic basis of learning as
"a change in the functional effectiveness of previously existing
excitatory connections

hebbian synapse

when two neurons fire at the same time, they become strengthened and
more likely to fire again in the future
cells that fire together, wire togethercells that fire
apart, wire apart
occurs when the successful stimulation of a cell by an axon leads
to the enhanced ability to stimulate that cell in the future

increased effectiveness of synaptic function occurs because:

a. increase in presynaptic transmitter release improves
nondeclarative STM b. increase in number of
post-synaptic receptors improves declarative STM
c. increased number of synapses improves LTM

long-term potentiation (LTP)

the enlargement of the graded potential; a mechanism of declarative LTM
when a number of axons are all firing on a dendrite for a period
of time, the neuron becomes more responsive to input of the same type
for a certain period of time


a decrease in response to a stimulus that is presented repeatedly
kandel ex: if you repeatedly stimulate an aplysia's gills with a
jet of seawater, at first it will withdraw, but eventually it will
stop responding


an increase in response to mild stimuli as a result of exposure to
more intense stimuli
kandel ex: a strong stimulus almost anywhere on aplysia's skin
intensifies a later withdrawal response to a touch


if some of the synapses of a cell have been highly active and others
have not, only the active ones become strengthened


simultaneous stimulation by 2 or more axons produces LTP much more
strongly than repeated stimulation by a single axon


pairing a weak input with a strong input enhances later responses to
a weak input

biochemical mechanisms of LTP

the pre-synaptic neuron releases lots of glutamate which binds to the
AMPA receptors on the post-synaptic neuron.
this extreme depolarization allows the magnesium blocking the
nearby NMDA receptor to displace, and glutamate to binds to the NMDA
receptors which allow sodium to flow through both AMPA and NMDA
receptors, and calcium to flow through NMDA receptors
this causes more post-synaptic receptors and more axons are made,
which allows for greater stimulaiton later on
this established LTP

short-term synaptic changes of LTP

repeated glutamate excitation causes more AMPA and NMDA receptors to
be made and put onto the surface of the post-synaptic neuron
this increases the responsiveness of the receptors on the
post-synaptic dendrite to incoming glutamate which leads to increased
synaptic strength

long-term synaptic changes of LTP

in response to the increased stimulation of a postsynaptic cell

learning and memory involves:

pre-synaptic cell changes - more neurotransmitters are released,
decrease in action potential threshold
post-synaptic cell changes - expansion of membrane - more
receptors and axons
more neurotransmitters can be released from more sites and
received at more sites

korsakoff's syndrome

more common in alcoholics - causes them to lose vitamins they need to
metabolize glucose, so neurons in the brain shrink
this causes damage to the prefrontal cortex leading to memory
loss and confusion, similar to those with hippocampal damage,
impairment of episodic and sparing of implicit memory
major symptom is confabulation - where they fill in missing
memories with wrong ones

alzheimer's disease

have better procedural than declarative memory, they learn new skills
but then surprise themselves at their skills because they don't
remember learning those skills
neurons weaken and die with causes memory loss

what stimulates an LTP

repeated huge release of neurotransmitters from a strong action potential

benefits of greater surface area following LTP

greater opportunity for receptors, collateral sprouting, axonal
endings � all part of synaptogenesis, when we are learning and storing
information, all of that is accompanied by structural changes in the brain


the private awareness we have of our emotions, intentions, thoughts,
sensations and movements
right now we cant stimulate parts of the brain to induce consciousness
machines cant be brought to experience awareness
consciousness exists in certain parts of certain kinds of nervous systems
we can only be aware of 1-2 thoughts at a time, so most of our
processing is non-conscious

neural correlates of consciousness

the relationship between the experiences reported by subjects and the
activity that simultaneously takes place in their brains

why do researchers study apes so much

they resemble many human characteristics
form social hierarchy relationships and exhibit competition for resources
this shows the evolution of intelligence


we are aware of ourselves and others and can learn about ourselves
from others' behavior
the product of a diffuse patchwork of key cortical regions
mirror and rouge task - put a mark on animals and humans to see
if they are able to recognize that the mark is actually yon
themselves and they can notice it

cerebral asymmetry

the idea that each brain hemisphere is specialized for different functions
right vs left hemisphere - perform different but complementary functions

left side is specialized for

logical/linear thinking, language, writing, science and math, speech
became specialized for handedness and then developed speech

right side is specialized for

musical and artistic ability, perception of space, imagination and
fantasizing, body control and awareness
3D space and more creative/abstract
thought to have specialized for the purpose of detecting and
responding to unexpected stimuli
essential for recognizing predators quickly, face recognition,
analyzing spatial relationships


the chimp that learned to sign and even went on to teach other chimps
to sign
used mainly his right hand, this shows that they have selective
reliance on the left side just like humans do

ability of bonobos

resemble humans more than any other primates
show better comprehension of human language
understand more than they can produce, use symbols/names to
describe objects, request items not seen, use symbols to describe
past events, make original creative requests


a condition in which there is severe language impairment

broca's aphasia (nonfluent aphasia)

a speech production deficit unrelated to auditory
dysfunction, people with brain damage suffer impaired language production
people who are deaf cannot make meaningful speech, but that is
related to an auditory dysfunction, not to a problem in Broca�s area (aphasia)

main problem in broca's aphasia

they have a problem with understanding when sentence structure is complicated
they have a problem in moving the muscles to
produce speech, not a comprehension problem

wernicke's aphasia (fluent aphasia)

speech comprehension deficit unrelated to auditory dysfunction
poor language comprehension and impaired ability to remember
names of objects
can still speak smoothly, damage to secondary auditory cortex

characteristics of wernicke's aphasia

articulate speech - speak smoothly except when they have to remember
the name of something
difficulty finding the right word (anomia) - ex:
they use thingamajig or "the thing we use to sweep"
poor language comprehension - trouble understanding spoken and
written speech


a lack of use of syntax in speech production and comprehension
speech requires great effort


difficulty recalling the names of objects, especially nouns


words may be meaningless combinations of syllables

pronunciation in broca's vs wernickes aphasia

brocas - poor
wenickes - unimpaired

content of speech in broca's vs wernickes aphasia

brocas - mostly nouns and verbs, omits prepositions and other
grammatical connectives
wernickes - grammatical but nonsensical, has trouble finding the
right word, especially nouns

comprehension in broca's vs wernickes aphasia

brocas - impaired if the meaning depends on complex grammar
wernickes - seriously impaired

conduction aphasia

a patient can both comprehend and articulate language, but cannot
verbalize what is a clear idea in their mind

geschwind disconnection theory

deficits can be understood as breaks in an interconnected network of
components, each is involved with a particular feature of language
analysis or production

corpus callosum

a set of axons that allow exchange of information between the left
and right hemispheres
right knows what the left is doing, and vice versa

split-brain operation

cut the corpus callosum to prevent epileptic seizures from spreading
to the opposite side of the brain

optic chiasm

part of the brain where half of the axons from each eye cross to the
opposite side of the brain
this allows info received from the left visual field to be
processed in the right, and info from the right visual field to be
processed on the left


division of labor between the two hemispheres of the brain

split brain patients

had their corpus callosum cut, but have two independent streams of consciousness
when a stimulus is presented in the right visual field, the
stimulus is transmitted to the visual area in the left hemisphere and
the person can recognize the stimulus
when a stimulus is presented in the left visual field, the
stimulus is transmitted to the visual area in the right hemisphere,
and the person cannot say what they see
however, motor and somatosensory areas of the right hemisphere
aloow the person to pick up or point to the object represented in the
stimulus with their left hand

inter-manual conflit

occurs in split brain patients when the hands act at cross-purposes -
left hand behaves in a "foreign or alien" manner
ex: woman trying to pick out dress, right and left hand pick 2
different dresses and she is unable to decide which to choose


filling in memory gaps with guesses
ex: video we watched of split brain patient guessing what the
woman was doing in the picture she saw that was presented on the left
side. she guessed jumprope when the woman was actually on the phone
we fill in the gaps with the best guess in the absence of information


when the right hemisphere communicates using non-verbal behavior with
the left hemisphere
ex: when "clap : laugh" was presented, the lady did both,
but did not realize she was clapping

why should the right side not be regarded as the minor hemisphere

it has different abilities, not less important ones

sequential similar

cognitive processes in time are blended and then perceived as one -
putting together static images into a sequence, our brain pieces it together
ex: pictures of little girl laughing and not laughing

sequential dissimilar

processes in time are assessed independently
ex: pictures of little girl laughing and then a picture of an old lady
we are able to recognize that the picture of the old lady does
not fit with the sequence of the rest of the pictures

Agenesis of corpus callosum

people born without a corpus callosum, but still function normally

where do awareness and comprehension occur

Awareness occurs in primary associative cortex
Comprehension in secondary associative cortex

the illusion of knowledge

Your brain creates the illusion that you know more that you actually
do so you can handle the things that come at you
this is a survival mechanism to make us feel more in control


the ability to increase or decrease activity of the engaged neurons
functioning to process the stimulus scene

selective attention

only reacting to certain stimuli and ignoring others when several are
presented simultaneously in order to accomplish tasks

rapid attentive systems

noticeable, readily perceived stimuli
transmitted from lower to high order (bottom-up)
ex: you see a bear, and the information that you just saw a bear is
sent up to your brain (amygdala, motor cortex), where you realize that
you are scared and need to run

slow attentive system

our brain making use of information that has already been brought
into the brain by other sensory systems
controlled from higher to lower order (top-down)

attentive biasing

involves increasing activity in some neural networks and decreasing
it in others - a top-down process

what parts of the brain control attention

the prefrontal cortex and secondary sensory associative cortex

fate of an unattended stimulus

some things capture your attention faster than other things (ex:
name, special word)
if a meaningful stimulus captures your attention faster than a
meaningless stimulus, somehow your brain had to know that it was
meaningful before it became conscious - shows that most brain activity
is unconscious, and even unconscious activity can influence behavior

spatial neglect

after brain damage to the right side - people are unable to notice or
be aware that there is something on their left

pathway of speech production

1. Sound comes in through the ear and sent to wernicke�s area
2. Sent to Broca�s area where sounds are broken apart
3. Sent to primary motor cortex, where the speech is then produced

major depressive disorder

feel sad and helpless every day for weeks at a time, little energy,
feel worthless, contemplate suicide, find little pleasure, cant
imagine being happy


a deteriorating ability to function in everyday life, and have
experienced delusions, hallucinations, disorganized speech and
behavior, absent emotion and socialization for more than 6 months
literally means "split-mind" but it is
not multiple personalities!

prevalence of schizophrenia

less than 1% of the population
cost in US exceeds cost of all cancers
more common in US and Europe than in 3rd world countries
severity is highly variable

2 types of schizophrenia

acute - condition has a sudden onset and good prospect for recovery
chronic - condition has a gradual onset, a long-term course and
poor prognosis

3 types of schizophrenic symptoms

positive, negative and cognitive

positive symptoms of schizophrenia

behaviors that are present that should be absent
ex: delusions, hallucinations, irrational thoughts

negative symptoms of schizophrenia

behaviors that are absent or diminished but should be present
ex: socialization, infrequent speech, absent emotion
these symptoms are usually stable over time and difficult to treat

cognitive symptoms

deficits in higher cerebral functioning; closely related to negative
symptoms and are characterized by higher cognitive difficulties
ex: poor problem solving, learning and memory, and abstract
thinking; difficulty sustaining attention; low psychomotor speed on
tasks where fingers/hands must move rapidly

types of positive symptoms in schizophrenia

psychotic - delusions and hallucinations
delusions - unfounded beliefs (god-like power) and persecution or
control (belief that someone is after them or trying to control them)
disorganized - inappropriate emotional displays, bizarre
behaviors, thought disorders (disorganized, irrational thinking;
difficulty in logic and sorting out plausible conclusions from absurd
choices; jump from one topic to the next in conversation)

symptom order of schizophrenia

negative symptoms -> cognitive symptoms -> positive symptoms

time course of schizophrenia

symptoms usually appear gradually over 3-5 years

hypothesis for abnormal brain development in schizophrenics

abnormalities in prenatal or neonatal development of the CNS leads to
subtle abnormalities of brain anatomy and major abnormalities in behavior
abnormalities could result from 1. genetics2. trouble
during prenatal/postnatal development or birth3. environmental
influences later in life

genetics/heritability of schizophrenia

appears to be heritable
monozygotic twins have a higher concordance rate than dizygotic
twins (48/17) but because it's only 48%, either there is one gene that
is influenced by other factors that increase susceptibility of it
being triggered, or multiple genes

the dopamine (DA) hypothesis of schizophrenia

positive symptoms are caused by an over-activity of dopamine neurons
in neural pathways connecting the ventral tegmentum to the nucleus
accumbens in the basal forebrain and then to the prefrontal cortex
when anti-DA medication (which has anti-anxiety side effects) were
used on schizophrenic patients, these medications relieved the symptoms

drug treatment: dopamine antagonists/agonists

thorazine is a dopamine antagonist (blocker) used to treat
schizophrenia, blocks dopamine receptors so positive symptoms can be lessened
L-DOPA, cocaine and amphetamines are dopamine agonists that have
an opposite effect and worsen positive symptoms
increased activity at the dopamine receptor in nucleus accumbens
drives positive symptoms

glutamate hypothesis

deficient NMDA receptor stimulation (by glutamate/glutamine) in the
glutaminergic neurons of the prefontal cortex may result in
over-activity (of neuronal response) of the tegmental-forebrain DA pathway
hence, low NMDA receptor stimulation results in increased symptoms
in schizophrenics

proof of glutamate hypothesis

PCP is an antagonist of NMDA receptors in the prefrontal cortex,
large PCP doses produce positive, negative and cognitive schizophrenic symptoms

neural connection for schizophrenic symptoms

lower activation (hypoactivity) of NMDA pathways in prefrontal cortex
(causes negative and cognitive symptoms) leads to greater activation
(hyperactivity) of forebrain dopamine pathways (causes positive symptoms)

non-genetic influences for depression

infections, hormones and stress

what helps depression

anti-depressant drugs (SSRI's and trycyclics) that block reuptake of
dopamine, norepinephrine and serotonin - effectiveness could be due to
placebo effect, or normal recovery over time
electroconvulsive therapy - an electrically induced seizure. lasts
for a few months but could lead to brain damage if done wrong

bipolar disorder

alternating between two poles - depression and mania
depression - sadness, helplessness, litte worthmania -
excitement, laughter, self-confidence, loss of inhibitions

seasonal affective disorder

depression the recurs during a particular season
most prevalent in the poles where there are long nights, most often
caused by a mutation in genes that regulate circadian rhythms